The purpose of this study is to define the immunological properties of bovine peripheral nerve myelin P2 protein, especially with regard to its ability to produce experimental allergic neuritis (EAN) in Lewis rats. By isolating immunogenic peptide fragments, we will localize the antigenic and neuritogenic determinants, and investigate the properties of these determinants. Using the P2 protein we will attempt to manipulate the immune response so as to affect and particularly to treat the disorder. We will also investigate the role of lymphocyte subsets in EAN by using monoclonal antibodies that define these subsets. We will investigate the ability of the monoclonal antibodies to affect the course of EAN produced both by active sensitization and by transfer of activated cells. We will study the role played by these lymphocyte subsets during transfer of EAN by treating donor cells with the monoclonal antibodies or by depleting various subpopulations by rosetting using monoclonal antibodies that define these subsets. We will also develop T cell lines that mediate EAN and study the effect of the monoclonal antibodies on the ability of the T cell lines to produce EAN. We will attempt to develop monoclonal antibodies to the T cell lines which can alter the course of EAN. We will also use the T cell lines to help define the neuritogenic determinant(s) of the P2 protein. We hope to be able to learn the best way to treat EAN with monoclonal antibodies and/or peptides in order to stop the disease or promote recovery. Since experimental allergic neuritis is the appropriate animal model for human idiopathic polyneuritis, we hope that this information can serve as a basis from which one can devise similar treatments of relevant human demyelinating diseases.